Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity
Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations,...
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| Autor*in: |
Grima, Gilbert [verfasserIn] Benz, Beatrix [verfasserIn] Do, Kim Q. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2001 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 14(2001), 11, Seite 0 |
| Übergeordnetes Werk: |
volume:14 ; year:2001 ; number:11 ; pages:0 |
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| DOI / URN: |
10.1046/j.0953-816x.2001.01799.x |
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| 520 | |a Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. | ||
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10.1046/j.0953-816x.2001.01799.x doi (DE-627)NLEJ242435149 DE-627 ger DE-627 rakwb Grima, Gilbert verfasserin aut Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| neuroprotection Benz, Beatrix verfasserin aut Do, Kim Q. verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 14(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:14 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 14 2001 11 0 |
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10.1046/j.0953-816x.2001.01799.x doi (DE-627)NLEJ242435149 DE-627 ger DE-627 rakwb Grima, Gilbert verfasserin aut Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| neuroprotection Benz, Beatrix verfasserin aut Do, Kim Q. verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 14(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:14 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 14 2001 11 0 |
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10.1046/j.0953-816x.2001.01799.x doi (DE-627)NLEJ242435149 DE-627 ger DE-627 rakwb Grima, Gilbert verfasserin aut Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| neuroprotection Benz, Beatrix verfasserin aut Do, Kim Q. verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 14(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:14 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 14 2001 11 0 |
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10.1046/j.0953-816x.2001.01799.x doi (DE-627)NLEJ242435149 DE-627 ger DE-627 rakwb Grima, Gilbert verfasserin aut Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| neuroprotection Benz, Beatrix verfasserin aut Do, Kim Q. verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 14(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:14 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 14 2001 11 0 |
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10.1046/j.0953-816x.2001.01799.x doi (DE-627)NLEJ242435149 DE-627 ger DE-627 rakwb Grima, Gilbert verfasserin aut Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| neuroprotection Benz, Beatrix verfasserin aut Do, Kim Q. verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 14(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:14 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 14 2001 11 0 |
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Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity |
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Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. |
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Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. |
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Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia. |
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10.1046/j.0953-816x.2001.01799.x |
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2024-07-06T01:59:41.444Z |
| _version_ |
1803793131316969472 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ242435149</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230505204357.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2001 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.0953-816x.2001.01799.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242435149</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Grima, Gilbert</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Glial-derived arginine, the nitric oxide precursor, protects neurons from NMDA-induced excitotoxicity</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2001</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Excitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l-arginine (L-Arg). At low L-Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L-Arg induces neuronal cell death, and that the presence of L-Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L-Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L-Arg. Indeed, as we further show, glial-derived L-Arg inhibits NMDA-induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L-Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2001</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2001||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">neuroprotection</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Benz, Beatrix</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Do, Kim Q.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">European journal of neuroscience</subfield><subfield code="d">Oxford [u.a.] : Blackwell, 1989</subfield><subfield code="g">14(2001), 11, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926383</subfield><subfield code="w">(DE-600)2005178-5</subfield><subfield code="x">1460-9568</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:14</subfield><subfield code="g">year:2001</subfield><subfield code="g">number:11</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.0953-816x.2001.01799.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">14</subfield><subfield code="j">2001</subfield><subfield code="e">11</subfield><subfield code="h">0</subfield></datafield></record></collection>
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7.3989096 |